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I read with interest the papers by Arnestad et al1 and Wang et al,2 as well as the editorial by Berul and Perry,3 which rekindle debate on neonatal assessment of long-QT syndrome as an underlying cause of sudden infant death syndrome. The authors appear to presume that ventricular fibrillation (VF) is responsible for the lethal event, and they liken this to sudden death in adults with ischemic and other cardiac disease.

As supervisor of cardiac activities in the ambulance service for the Australian state of New South Wales (population, 6.3 million), I had the opportunity to review 12 490 cases of sudden cardiac arrest in which ECG monitoring was performed with defibrillator pads or paddles.4 VF was the original rhythm in 40% of adults, but in <5% of young children. Hospital survival for VF in adults was ≈13% but zero for infants over the 10-year period.

Our findings provide no enthusiasm for mass ECG or genetic screening, or for focus on tachyarrhythmia with consideration of β-blocker therapy or defibrillator implant. Findings do support the majority view that a respiratory event is the primary cause of most sudden infant death syndrome cases. Attention to respiratory issues (ie, position in crib, location of pillow and bedclothes, passive smoking) have led to a dramatic fall in the occurrence of sudden infant death syndrome in Australia.5

Before health authorities promote any screening or treatment plan aimed at prevention of VF in infants, it is desirable that they first question their assumptions and provide evidence that infantile VF is a correctable problem in society.